Chronic hepatitis significantly increases the risk of liver cancer, especially in older adults, through a complex interplay of ongoing liver inflammation, cellular damage, and genetic changes that accumulate over time. The two most common chronic hepatitis infections linked to liver cancer are hepatitis B virus (HBV) and hepatitis C virus (HCV), both of which cause persistent infection in the liver that can lead to serious complications including cirrhosis and hepatocellular carcinoma (HCC), the primary form of liver cancer.
When someone has chronic hepatitis, their immune system continuously fights the viral infection in the liver. This prolonged immune response causes repeated cycles of inflammation and healing. Over many years or decades—often longer in older adults—this cycle damages healthy liver cells and leads to scarring known as fibrosis. As fibrosis worsens into cirrhosis, normal tissue is replaced by stiff scar tissue that disrupts normal blood flow and impairs liver function.
This damaged environment creates fertile ground for cancer development because:
– **Chronic inflammation produces harmful molecules** such as free radicals that damage DNA inside liver cells. This genetic damage can cause mutations activating oncogenes or disabling tumor suppressor genes—key steps toward malignant transformation.
– **Repeated cell death triggers compensatory regeneration**, causing surviving hepatocytes to divide rapidly to replace lost cells. Each round of cell division carries a risk for replication errors leading to further mutations.
– **The fibrotic scar tissue alters cellular signaling** pathways controlling growth and death, promoting an environment where abnormal cells can survive longer than they should.
In HBV infection specifically, the virus integrates its DNA into host hepatocyte genomes. This integration itself can disrupt normal gene function or activate oncogenes directly contributing to carcinogenesis independent from cirrhosis development. Additionally, HBV produces proteins like HBsAg (hepatitis B surface antigen) which interfere with cellular processes regulating growth control and apoptosis (programmed cell death).
For HCV infection, although it does not integrate into host DNA like HBV does, it induces oxidative stress within infected hepatocytes along with persistent inflammation that promotes genetic instability over time.
Older adults are at higher risk because these processes take many years before enough cumulative damage occurs for cancerous transformation:
– The longer duration since initial infection allows more cycles of injury-regeneration-inflammation.
– Aging itself reduces cellular repair mechanisms making DNA damage more likely to persist.
– Older livers may have additional insults such as fatty infiltration or metabolic dysfunctions compounding injury.
Once cirrhosis develops—a common endpoint for chronic hepatitis—the risk escalates dramatically since cirrhotic nodules frequently harbor pre-cancerous changes setting the stage for HCC emergence.
Moreover, recent research shows molecular alterations during this progression include epigenetic modifications affecting gene expression without changing DNA sequence but still promoting tumor formation; altered metabolism favoring rapid tumor growth; decreased detoxifying enzyme activity reducing protection against carcinogens; all contributing layers increasing malignancy likelihood in chronically inflamed livers.
In summary: Chronic hepatitis leads to continuous immune-mediated attack on the liver causing progressive scarring combined with direct viral effects on genes inside hepatocytes plus age-related decline in repair capacity—all converging over years primarily in older adults—to increase mutation accumulation driving malignant transformation culminating often as hepatocellular carcinoma.